Few studies have been performed to investigate the effect of vitamin D supplementation and T2DM in type 2 diabetic animal models. The present study aimed to explore the relationship between early 1,25-dihydroxyvitamin D [1,25(OH)D] and the incidence of T2DM and determine whether early 1,25(OH)D supplementation was associated with inflammation in KK-A mice. The KK-A mice were divided into 4 vitamin D treatment groups, the low-dose vitamin D supplementation group (VDS-L, 1.5 μg/kg 1,25(OH)D), moderate-dose vitamin D supplementation group (VDS-M, 3.0 μg/kg 1,25(OH)D), high-dose vitamin D supplementation group (VDS-H, 6.0 μg/kg 1,25(OH)D) and the model control group (MC). C57BL/6J mice were used as the controls. The treatment period lasted for 9 wk. During this treatment period, fasting blood glucose (FBG) level of the mice was measured on a weekly basis. The levels of lipid profile, insulin and inflammation biomarkers were determined after 9 wk of 1,25(OH)D intragastric gavage. After 9 wk of 1,25(OH)D intragastric gavage, FBG level was significantly decreased in the vitamin D treatment groups compared with the MC group. The number of T2DM incidence in the VDS-L group (n=7), VDS-M group (n=5) and VDS-H group (n=3) was lower than those in the MC group (n=10) on week 9. Moreover, serum C-reactive protein (CRP) and interleukin-6 (IL-6) in the vitamin D treatment groups were significantly suppressed by 1,25(OH)D administration compared with the MC group. Early 1,25(OH)D supplementation could effectively lower the incidence of T2DM via ameliorating inflammation in KK-A mice.
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http://dx.doi.org/10.3177/jnsv.67.84 | DOI Listing |
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